lipidLev Cancer Research Results

lipidLev, Lipid Levels: Click to Expand ⟱

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Type:

Lipid levels refer to the concentration and distribution of various lipids—including fatty acids, cholesterol, phospholipids, and triglycerides—in cells and tissues. Lipids are essential components of cellular membranes, serve as energy storage molecules, and act as signaling molecules that regulate cellular processes such as growth, apoptosis, and inflammation.

Under normal physiological conditions, lipid levels are tightly regulated by dietary intake, de novo synthesis, uptake, storage, and breakdown. Enzymes (e.g., fatty acid synthase, acetyl-CoA carboxylase) and transcription factors (e.g., SREBP1) coordinate these processes to maintain cellular homeostasis.

Many tumors upregulate de novo lipogenesis to generate lipids internally, even in the presence of exogenous lipids. As a result, cancer cells often have elevated levels of fatty acids and other lipid intermediates. These adjustments not only support rapid growth but also contribute to resistance to stress and apoptosis.

Scientific Papers found: Click to Expand⟱

2782-

CHr,

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

Review,

Var,

Review,

Stroke,

Review,

Park,

*antiOx↑, antioxidant, anti-inflammatory, hepatoprotective, neuroprotective
*Inflam↓, inhibitory effect of chrysin on inflammation and oxidative stress is also important in Parkinson’s disease
*hepatoP↑,
*neuroP↑,
*BioAv↓, Accumulating data demonstrates that poor absorption, rapid metabolism, and systemic elimination are responsible for poor bioavailability of chrysin in humans that, subsequently, restrict its therapeutic effects
*cardioP↑, cardioprotective [69], lipid-lowering effect [70]
*lipidLev↓,
*RenoP↑, Renoprotective
*TNF-α↓, chrysin reduces levels of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-2 (IL-2).
*IL2↓,
*PI3K↓, induction of the PI3K/Akt signaling pathway by chrysin contributes to a reduction in oxidative stress and inflammation during cerebral I/R injury
*Akt↓,
*ROS↓,
*cognitive↑, Chrysin (25, 50, and 100 mg/kg) improves cognitive capacity, inflammation, and apoptosis to ameliorate traumatic brain injury
eff↑, chrysin and silibinin is beneficial in suppressing breast cancer malignancy via decreasing cancer proliferation
cycD1/CCND1↓, chrysin and silibinin induced cell cycle arrest via down-regulation of cyclin D1 and hTERT
hTERT/TERT↓,
VEGF↓, Administration of chrysin is associated with the disruption of hypoxia-induced VEGF gene expression
p‑STAT3↓, chrysin is capable of reducing STAT3 phosphorylation in hypoxic conditions without affecting the HIF-1α protein level.
TumMeta↓, chrysin is a potent agent in suppressing metastasis and proliferation of breast cancer cells during hypoxic conditions
TumCP↓,
eff↑, combination therapy of breast cancer cells using chrysin and metformin exerts a synergistic effect and is more efficient compared to chrysin alone
eff↑, combination of quercetin and chrysin reduced levels of pro-inflammatory factors, such as IL-1β, Il-6, TNF-α, and IL-10, via NF-κB down-regulation.
IL1β↓,
IL6↓,
NF-kB↓,
ROS↑, after chrysin administration, an increase occurs in levels of ROS that, subsequently, impairs the integrity of the mitochondrial membrane, leading to cytochrome C release and apoptosis induction
MMP↓,
Cyt‑c↑,
Apoptosis↑,
ER Stress↑, in addition to mitochondria, ER can also participate in apoptosis
Ca+2↑, Upon chrysin administration, an increase occurs in levels of ROS and cytoplasmic Ca2+ that mediate apoptosis induction in OC cells
TET1↑, In MKN45 cells, chrysin promotes the expression of TET1
Let-7↑, Chrysin is capable of promoting the expression of miR-9 and Let-7a as onco-suppressor factors in cancer to inhibit the proliferation of GC cells
Twist↓, Down-regulation of NF-κB, and subsequent decrease in Twist/EMT are mediated by chrysin administration, negatively affecting cervical cancer metastasis
EMT↓,
TumCCA↑, nduction of cell cycle arrest and apoptosis via up-regulation of caspase-3, caspase-9, and Bax are mediated by chrysin
Casp3↑,
Casp9↑,
BAX↑,
HK2↓, Chrysin administration (15, 30, and 60 mM) reduces the expression of HK-2 in hepatocellular carcinoma (HCC) cells to impair glucose uptake and lactate production.
GlucoseCon↓,
lactateProd↓,
Glycolysis↓, In addition to glycolysis metabolism impairment, the inhibitory effect of chrysin on HK-2 leads to apoptosis
SHP1↑, upstream modulator of STAT3 known as SHP-1 is up-regulated by chrysin
N-cadherin↓, Furthermore, N-cadherin and E-cadherin are respectively down-regulated and up-regulated upon chrysin administration in inhibiting melanoma invasion
E-cadherin↑,
UPR↑, chrysin substantially diminishes survival by ER stress induction via stimulating UPR, PERK, ATF4, and elF2α
PERK↑,
ATF4↑,
eIF2α↑,
RadioS↑, Irradiation combined with chrysin exerts a synergistic effect
NOTCH1↑, Irradiation combined with chrysin exerts a synergistic effect
NRF2↓, in reducing Nrf2 expression, chrysin down-regulates the expression of ERK and PI3K/Akt pathways—leading to an increase in the efficiency of doxorubicin in chemotherapy
BioAv↑, chrysin at the tumor site by polymeric nanoparticles leads to enhanced anti-tumor activity, due to enhanced cellular uptake
eff↑, Chrysin- and curcumin-loaded nanoparticles significantly promote the expression of TIMP-1 and TIMP-2 to exert a reduction in melanoma invasion

2788-

CHr,

Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of action

Review,

Var,

*neuroP↑, Chrysin mitigates neurotoxicity, neuroinflammation, and oxidative stress.
*Inflam↓,
*ROS↓,
NF-kB↓, Chrysin treatment maintains the antioxidant armory and suppresses the activation of redox-active transcription factor NF-kB
*PCNA↓, Chrysin supplementation downregulated the expression of PCNA, COX-2, and NF-kB
*COX2/PTGS2↓,
ChemoSen↑, Chrysin is effective in attenuating cisplatin-induced expression of both COX-2 and iNOS
Hif1a↓, DU145: Chrysin suppressed the expression of HIF-1a of tumor cells in vitro and inhibited tumor cell-induced angiogenesis in vivo
angioG↓,
*chemoPv↑, Chrysin as an effective chemopreventive agent having the capability to obstruct DEN initiated and Fe-NTA promoted renal cancer in the rat model
PDGF↓, Chrysin functionally suppresses PDGF-induced proliferation and migration in VSMCs
*memory↑, Chrysin is effective in attenuating memory impairment, oxidative stress, acting as an antiaging agent
*RenoP↑, protected the kidney from damage
*PPARα↑, Chrysin significantly inhibits AGE-RAGE mediated oxidative stress and inflammation through PPAR-g activation
*lipidLev↓, Chrysin was able to decrease plasma lipids concentration because of its antioxidant properties
*hepatoP↑, Chrysin shows promising hepatoprotective and antihyperlipidemic effects, which are evidenced by the decreased levels of triglycerides, free fatty acids, total cholesterol, phospholipids, low-density lipoprotein-C, and very low-density lipoprotein
*cardioP⇅, Chrysin significantly ameliorated myocardial damage
*BioAv↓, despite its therapeutic potential, the bioavailability of chrysin and probably other flavonoids in humans is extremely low, mainly due to poor absorption, rapid metabolism, and rapid systemic elimination.

6571-

Ger,

Unlocking the therapeutic potential of Geraniol: an alternative perspective for metabolic disease management

Review,

Obesity,

*lipidLev↓, Recent research has demonstrated the lipid-lowering, antioxidant, and anti-inflammatory properties of geraniol as well as its ability to improve endothelial function and reduce oxidative stress in preclinical animals.
*antiOx↓,
Inflam↓,
*ROS↓,
*BioAv↑, The paper delves into the various nanoformulations, including liposomes, nanoparticles, and nanoemulsions, which enhance geraniol's therapeutic efficacy and bioavailability, making it a viable option for managing metabolic syndrome.
*AntiDiabetic↑, which makes it a compelling option for the treatment of conditions such as neuroinflammation, diabetes, and obesity.
*Obesity↓,

7744-

ISL,

Isoliquiritigenin suppresses fatty acid synthesis and cancer cell migration in anaplastic thyroid carcinoma through AMPK/SREBF1 pathway

vitro+vivo,

Thyroid,

 tumor xenografts in mice

AntiTum↑, Isoliquiritigenin (ISL), a bioactive isoflavonoid, has exhibited an antitumor activity across multiple tumor types;
TumCP↓, The results showed that ISL effectively hindered the proliferation of ATC cells, inhibited cancer cell migration by up-regulating the level of E-cadherin and down-regulating the level of N-cadherin,
TumCMig↓,
E-cadherin↑,
N-cadherin↓,
FASN↓, and inhibited fatty acid synthesis by down-regulating the level of Sterol regulatory element binding transcription factor 1 (SREBF1) and its downstream lipid synthesis-related enzyme expression level.
SREBP1/SREBF1↓,
ATP↓, The underlying mechanism appears to involve a decrease in intracellular ATP levels induced by ISL and the activation of phosphorylated AMPK, thereby downregulating the expression of SREBF1,
p‑AMPK↑,
lipidLev↓, ultimately inhibiting cell proliferation, migration, and lipid synthesis
TumCG↓, In vivo experiments further confirmed that ISL significantly retarded the growth of tumor xenografts in mice, diminished tumor cell proliferation, and reduced SREBF1 protein levels.
lipoGen↓, ISL modulates lipogenesis and impedes cancer cell migration in ATC through the AMPK/SREBF1 signaling pathway.

7757-

ISL,

Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism: Association with the circPOLB/miR-548ae-3p/C-MYC Axis

in-vitro,

Oral,

FABP5/E-FABP↓, ISL treatment decreased FABP5 expression, fatty acid metabolism, and invasive capacity of OSCC cells (n = 3, p < 0.001), supporting its potential as a therapeutic agent.
FAM↓,
TumCI↓,
lipidLev↓, Targeting lipid metabolism using agents like ISL could be a promising approach for treating OSCC.

8080-

KAE,

Hepatoprotective Effect of Kaempferol—A Review

Review,

Nor,

*hepatoP↑, Kaempferol, a naturally occurring flavonoid, has demonstrated significant hepatoprotective effects in preclinical models
*SIRT1↑, This substance activates the SIRT1/AMPK signalling pathway, improves mitochondrial function, inhibits proinflammatory cytokine production via TLR4/NF-κB suppression and attenuates hepatic stellate cell activation by modulating the TGF-β/Smad pathwa
*AMPK↑,
*TLR4↓,
*NF-kB↓,
*GutMicro↑, kaempferol regulates the composition of the gut microbiota, thus improving bile acid metabolism and alleviating steatosis and fibrosis.
*Dose↝, The most significant amounts of kaempferol can be found in vegetables such as kale, spinach, onions, or beverages, especially black or green tea infusions
*BioAv↓, the bioavailability of the various chemical forms of oral kaempferol is low and has been calculated to be around 2%
*BioAv↑, However, there are some modern approaches (nanoparticles, structural modifications, chimeric molecules) that could certainly be exploited to improve kaempferol bioavailability [
*CYP2E1↓, including SIRT1 activation, CYP2E1 inhibition, TLR4/NF-κB suppression and ALK5/Smad pathway interference
*lipidLev↓, Reduction of Hepatic Lipid Accumulation
*COX2/PTGS2↓, Kaempferol can also suppress the production and expression of COX-2, IL-1β, TNF-α, and IL-6 mRNA, which play key roles in inflammation
*IL1β↓,
*TNF-α↓,
*IL6↓,
*NO↓, reduces the levels of NO and PGE2 while lowering iNOS mRNA expression in cases of acute liver injury.
*PGE2↓,
*iNOS↓,
*SOD↑, increased SOD activity and decreased MDA levels in the liver were observed when compared with the haemorrhagic shock group.
*MDA↓,
*ROS↓, inhibit CYP2E1 at both the expression and activity levels, consequently leading to a reduction in ROS levels and liver damage.
*AST↓, The significant decrease in serum AST and ALT levels is due to this inhibitory effect.
*ALAT↓,
*GSH↑, The induction of reactive antioxidant enzymes (GSH and SOD) by this compound
*SOD↑,
*Cyt‑c↓, inhibiting hepatocyte apoptosis through the reduction of apoptosis-related proteins, including cytochrome c, Bax, Bcl-2, caspases:3, 8 and 9
*BAX↓,
*Casp3↓,
*Casp8↓,
*Casp9↓,
*COL1↓, Kaempferol has been shown to be capable of inhibiting type I collagen expression in HSCs and reducing collagen density in liver tissue
*p‑SMAD2↓, reducing the phosphorylation of Smad2 and Smad3 by the serine/threonine kinase, attenuating α-SMA production, and inhibiting TGF-β-stimulated HSCs
*p‑SMAD3↑,
*α-SMA↓,
*TGF-β↓,
*P450↝, Kaempferol interacts with cytochrome P450 enzymes, including CYP3A4, which is key to drug metabolism.
*P-gp/ABCB1↓, It has been demonstrated that kaempferol is capable of inhibiting P-gp, which may consequently result in an enhancement of the bioavailability of drugs that are P-gp substrates.
*BioEnh↑,

8155-

lamb,

Ethanol extract of Pinus koraiensis leaves containing lambertianic acid exerts anti-obesity and hypolipidemic effects by activating adenosine monophosphate-activated protein kinase (AMPK)

vitro+vivo,

Nor,

3T3

*p‑AMPK↑, LA induced the expression of p-AMPK and inhibited PPARγ, C/EBP α, adiponectin, FAS, SREBP-1, and HMGCR expression.
*PPARγ↓,
*CEBPA↓,
*adiP↓,
*Fas↓,
*SREBP1/SREBF1↓,
*HMGCR↓,
*lipidLev↓, EPK containing LA significantly decreased lipid accumulation and triglyceride levels in the differentiated 3 T3-L1 cells.
*TG/TAG↓,
*Weight↓, In vivo analysis showed that body weight gain, serum triglyceride, total cholesterol, LDL cholesterol and AI value in the EPK treatment group were lower than those in the HFD control group.
*LDL↓,
*Obesity↓, Overall, the results suggest that EPK containing LA exerts significant anti-obesity and cholesterol-lowering effects by activating AMPK

8150-

lamb,

Reactive oxygen species dependent phosphorylation of the liver kinase B1/AMP activated protein kinase/ acetyl-CoA carboxylase signaling is critically involved in apoptotic effect of lambertianic acid in hepatocellular carcinoma cells

in-vitro,

HCC,

HepG2

in-vitro,

HCC,

SK-HEP-1

lipidLev↓, Though lambertianic acid (LA) is reported to have hypolipidemic activity in liver
TumCCA↑, LA increased cytotoxicity, sub-G1 population and Annexin V/PI positive cells in two HCC cells
cl‑Casp3↑, LA cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP), activated phosphorylation of liver kinase B1 (LKB1)/AMP activated protein kinase (AMPK)/ acetyl-CoA carboxylase (ACC) pathway
cl‑PARP↑,
AMPK↑,
Akt↓, also suppressed antiapoptotic proteins such as phosphorylation of Akt/ mammalian target of rapamycin (mTOR) and the expression of B cell lymphoma-2 (Bcl-2)/ B-cell lymphoma-extra large (Bcl-xL) and cyclooxygenase-2 (COX-2) in two HCC cells.
mTOR↓,
Bcl-2↓,
Bcl-xL↓,
COX2/PTGS2↓,
ROS↑, LA generated reactive oxygen species (ROS) in HepG2 cells
eff↓, AMPK inhibitor compound C or ROS inhibitor N-acetyl-L-cysteine (NAC) blocked the apoptotic ability of LA to cleave PARP or increase sub G1 population in HepG2 cells.
p‑STK11/LKB1↑, Overall, these findings suggest that ROS dependent phosphorylation of LKB1/AMPK/ACC signaling is critically involved in LA induced apoptosis in HCCs.
p‑ACC↑,
*Obesity↓, labmertianic acid (LA) is known to have anti-obesity [40], stress-protective [41], anti-allergic [42] and neurotropic
*Stress↓,
*antiAll↑,
tumCV↓, LA significantly suppressed the viability of HepG2, SK-Hep1 and Hep3B cells in a concentration dependent fashion, but not Chang normal hepatocyte cells.
selectivity↑,
TumCP↓, LA significantly inhibited proliferation of two HCC cells in a concentration and time dependent manner

1191-

SM,

Salvia miltiorrhiza extract inhibits TPA‑induced MMP‑9 expression and invasion through the MAPK/AP‑1 signaling pathw

in-vitro,

BC,

MCF7

Inflam↓,
MMP9↓,
TumCI↓,
AP-1↓,
lipidLev↓,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,
Total Targets: 73

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

antiAll↑, 1, Stress↓, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 1, CYP2E1↓, 1, GSH↑, 1, MDA↓, 1, ROS↓, 4, SOD↑, 2,

Core Metabolism/Glycolysis(tgid=4) ⓘ

adiP↓, 1, ALAT↓, 1, AMPK↑, 1, p‑AMPK↑, 1, LDL↓, 1, lipidLev↓, 5, PPARα↑, 1, PPARγ↓, 1, SIRT1↑, 1, SREBP1/SREBF1↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, BAX↓, 1, Casp3↓, 1, Casp8↓, 1, Casp9↓, 1, Cyt‑c↓, 1, Fas↓, 1, iNOS↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

PCNA↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CEBPA↓, 1, HMGCR↓, 1, PI3K↓, 1,

Migration(tgid=13) ⓘ

COL1↓, 1, p‑SMAD2↓, 1, p‑SMAD3↑, 1, TGF-β↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2, IL1β↓, 1, IL2↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 2,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3, BioAv↑, 2, BioEnh↑, 1, Dose↝, 1, P450↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, AST↓, 1, GutMicro↑, 1, IL6↓, 1, TG/TAG↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1, cardioP↑, 1, cardioP⇅, 1, chemoPv↑, 1, cognitive↑, 1, hepatoP↑, 3, memory↑, 1, neuroP↑, 2, Obesity↓, 3, RenoP↑, 2, Weight↓, 1,
Total Targets: 68

Scientific Paper Hit Count for: lipidLev, Lipid Levels

2 Chrysin
2 Isoliquiritigenin
2 lambertianic acid
1 Geraniol
1 Kaempferol
1 Salvia miltiorrhiza

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1039  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

lipidLev Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

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